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72 Cards in this Set
- Front
- Back
TOUCH Prescribing Program associated with Natalizumab (Tysabri)
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1. prescribers and patients enrolled can prescribe and receive
2. certain pharmacies and infusion sites authorized can dispense and infuse 3. must re-authorize treatment every 6 months |
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Mechanism of Action of Mitoxantrone (Novantrone)
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*IMMUNOSUPPRESSANT*
1. inhibits the proliferation of T-cells, B-cells, and macrophages; impairs the secretion of molecules that promote inflammation |
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Clinical Use of Mitoxantrone (Novantrone)
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rapidly advancing MS disease who have failed other therapies
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Major Contraindication for Mitoxantrone (Novantrone)
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Cardiac Toxicity which can lead to CHF - must limit the amount per lifetime
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Patient Education for Mitoxantrone (Novantrone)
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1. Monitor for heart failure symptoms
2. monitor for symptoms of myelosuppression 3. blue-green urine color and bluish discoloration of sclera |
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Monitoring for Mitoxantrone (Novantrone)
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1. Weight
2. LVEF (left ventricular ejection fraction) 3. CBC 4. LFTs 5. pregnancy test |
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Mechanism of Action of Fingolimod (Gilenya)
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reduction of lymphocyte migration into the CNS
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Clinical use of Fingolimod (Gilenya)
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relapsing forms of MS; use as first or second-line therapy
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Pregnancy Category for Fingolimod (Gilenya)
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C - must use contraception during and for 2 months after stopping treatment
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Monitoring for Fingolimod (Gilenya)
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1. Bradycardia - electrocardiogram
2. Infections - CBC 3. Macular Edema - eye exams 4. Respiratory Effects - spirometric evaluation 5. Hepatic Effects - LFTs |
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Positive Lifestyle and Psychosocial for MS
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1. very low saturated and vit D supplementation
2. minimal, regular sunlight exposure 3. positive mental and social health and coping 4. exercise |
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Risk Factors for Parkinson's
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1. 1st degree relative
2. rural living 3. drinking well water 4. heavy metal, hydrocarbon, pesticide exposure 5. male |
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Pathophysiology of Parkinson's
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* Dopamine stores are depleted
* Nigrostiatal pathways destroyed * Imbalance of ACh, DA, GABA, Serotonin, etc **Excess of ACh and a deficiency of DA |
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General HallMark Symptoms of Parkinson's
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1. Rigidity
2. Resting Tremor 3. Bradykinesia |
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Motor Features of Parkinson's
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1. Decreased dexterity
2. Difficulty speaking(dysarthria) and swallowing(dysphagia) 3. Quiet speaking(hypophonia), hypomimia(few facial expressions), micrographia(small writing) 4. Festinating Gait |
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Autonomic Features of Parkinson's
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1. bladder disorder
2. constipation 3. fatigue 4. Skin problem(seborrhea) 5. Excessive salivating/drooling(sialorrhea) 6. orthostatic hypotension |
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Psychiatric Features of Parkinson's
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1. anxiety
2. apathy 3. confusion 4. insomnia 5. depression |
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Diagnosis of Parkinson's
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1. 2 of 3 hallmark features
2. response to pharmacotherapy |
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Initial Signs and Symptoms of Parkinson's
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*Insidious onset
*usually sensory symptoms and tremor *little impairment of activities *no pharmacotherapy required |
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Advanced Signs and Symptoms of Parkinson's
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*greater impairment of daily activities, quality of life
*psychiatric changes requiring additional pharmacotherapy *hypomobility akinesia |
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Goals of Treatment of Parkinson's
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1. Improve motor and non-motor function
2. maintain quality of life 3. avoid drug-induced complications |
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Non-Pharmacological Treatments of Parkinson's
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1. Exercise
2. Nutrition 3. Education 4. Support Groups 5. Neurosurgery |
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Anticholinergics used to treat Parkinson's
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1. Benztropine (Cogentin)
2. Trihexyphenidyl (Artane) |
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MAO-B Inhibitors used to treat Parkinson's
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1. Selegiline (Eldepryl, Zelapar)
2. Rasagiline (Azilect) |
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COMT Inhibitors used to treat Parkinson's
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1. Entacapone (Comtan)
2. Tolcapone (Tasmar) |
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Dopamine Agonists used to treat Parkinson's
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1. Bromocriptine (Parlodel)
2. Ropinirole (Requip) 3. Pramipexole (Mirapex) 4. Apomorphine (Apokyn) |
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Other Medications used to treat Parkinson's
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1. Carbidopa (Lodosyn)
2. Carbidopa/Levodopa (Sinemet, Parcopa) 3. Carbidopa/Levodopa/Entacapone (Stalevo) 4. Amantadine (Symmetrel) |
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Mechanism of Action of Anticholinergics for Parkinson's
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overcomes the increased cholinergic activity
*balances ACh and DA* |
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Indication for Anticholinergics for Parkinsons
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alone or as adjunct therapy
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Clinical Pearls for Anticholinergics
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1. most useful for tremor
2. sometimes useful for dystonia 3. little benefit for other clinical features 4. avoid use in elderly (over 65 years) |
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Possible MOA for Amantadine
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increases DA release, inhibits DA reuptake, stimulates DA receptors or inhibits NMDA
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Indication for use of Amantadine
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Monotherapy or Symptomatic and adjunct treatment
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ADRs for Amantadine
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CV: orthostatic hypotension, peripheral edema
CNS: confusion, hallucinations, insomnia, agitation GI: constipation, nausea, xerostomia Derm: livedo reticularis Dry Nose |
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Clinical Pearls for Amantadine
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1. useful in early, mild disease
2. benefit for tremor, rigidity, bradykinesia 3. renally dosed |
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MOA of Levodopa
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direct precursor to dopamine
1. penetrates CNS and is converted to dopamine by CENTRAL L-amino acid decarboxylase 2. can also be converted by PERIPHERAL L-amino acid decarboxylase and cannot enter CNS |
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MOA of Carbidopa
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L-amino acid decarboxylase inhibitor - allows levodopa to escape conversion in the periphery
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Indication for Levodopa/Carbidopa
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Treatment in both early and late stages
*ultimately all patients will be on it |
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ADRs of Levodopa/Carbidopa
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CV: arrhythmia(more common with levodopa alone), chest pain, orthostatic hypotension
CNS: anxiety, depression, abnormal dreams, hallucinations, confusion GI: ab pain, diarrhea, constipation, nausea, vomit |
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Max dose of Carbidopa
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200mg
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Max dose of Levodopa
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2000mg
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Clinical Pearls for Levodopa/Carbidopa
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1. most effective treatment
2. dyskinesias and other motor complications are common 3. akinesia improves rapidly & tremor/rigidity respond well. Balance/gain may not improve |
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Complications of DA therapy (levodopa/carbidopa)
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1. Delayed-On or No-On
2. Wearing Off 3. On/Off 4. Dyskinesias 5. Freezing 6. Dystonias 7. Myclonus 8. Akathisia |
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"Delayed-On" or "No-On"
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Signs: delayed or minimal response to previously effective dose
Treatment: give on empty stomach, chew or crush tab, switch to ODT, increase dose, add DA agonist |
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"Wearing off"
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Signs: decreased duration of response; occurs at end of dose
Treatment: change to CR prep, increase frequency, add MAOB inhibitor or DA agonist or COMT inhibitor, long acting agents at night |
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"On/Off"
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Signs: fluctuations from normal/good to poor movement
Treatment: add DA agonist, switch from IR to CR, add MAOB or COMT inhibitor |
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Dyskinesias
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Signs: abnormal involuntary jerking of face, neck, arms, legs
Treatment: decrease dose, change to CR prep, add amantadine |
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"Freezing"
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Signs: temporary, sudden, involuntary inability to move (usually lower extremities)
Treatment: increase dose, add DA agonist or MAOB inhibitor, physical therapy |
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Dystonias
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Signs: sustained muscle contraction in early morning
Treatment: add DA agonist, dose CR at bedtime, baclofen |
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Myoclonus
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Signs: repetitive jerking movements at night
Treatment: decrease nighttime dose, clonazepam |
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Akathisia
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Signs: restless feeling
Treatment: add nighttime dopaminergic med |
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MOA of MAO-B inhibitor
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selectively inhibits MAOa in the brain = inhibits DA degradation = enhanced dopaminergic activity
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Indication of use for MAO-B inhibitor
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1. adjunct therapy
2. initial monotherapy in early PD |
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Clinical Pearls with MAO-B Inhibitors
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1. often used as initial monotherapy with mild symptoms
2. bioavailability is increased with ODT |
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ADRs of MAO-B Inhibitors
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CNS: mood changes, insomnia, dizziness
GI: nausea, vomiting Neuromuscular: dyskinesias |
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Warnings with MAO-B inhibitors
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absolute contraindication with meperidine (Serotonin Syndrome)
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MOA of COMT inhibitors
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inhibit peripheral and central conversion of levodopa to dopamine by inhibiting catechol-o-methyltransferase enzyme
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Indication for use of COMT Inhibitors
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for combination therapy only, not first line
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Warnings for COMT inhibitors (tolcapone)
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fatal hepatotoxicity (reserved for last line)
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ADRs of COMT inhibitors
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CV: orthostatic hypotension, syncope
CNS: dizziness, fatigue, hallucination, anxiety GI: nausea, vomit, diarrhea, constipation Urinary: brown-orange urine color (COUNSEL) Neuromuscular: dyskinesias, muscle cramps, stiffness |
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Clinical Pearls for COMT inhibitors
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1. can allow a lower dose of levodopa
2. delayed onset of diarrhea (weeks to months later) 3. monitor LFTs at baseline then q2-4 week for 6 months |
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MOA of dopamine agonists
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directly stimulate DA receptors
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Indication of use for Dopamine agonists
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initial monotherapy or adjunctive therapy to carbidopa/levodopa
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ADRs of Dopamine Agonists
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CV: orthostatic hypotension, edema, chest pain
CNS: somnolence, insomnia, dizziness, hallucinations GI: nausea, constipation Neuromuscular: dyskinesia, weakness |
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Dopamine agonist with highest incidence of ADRs
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bromocriptine
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Dopamine agonist that can be used as "rescue therapy" by subq injection
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apomorphine
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Clinical Pearls of Dopamine agonists
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1. longer duration of action than levodopa & fewer motor complications
2. non-ergot agents have fewer ADRs 3. apomorphine requires pretreatment with trimethobenzamide(Tigan) |
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Essential Tremor
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disorder of the nervous system that causes involuntary shaking movements that can affect any part of the body but usually the hands
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Symptoms of Essential Tremor
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1. small, rapid movements (5+ times per second)
2. "yes-yes" or "no-no" motion of head 3. shaking or quivering speech |
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Non Pharm Treatment of Essential Tremor
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1. Relaxation techniques
2. avoid caffeine 3. use alcohol sparingly 4. obtain enough rest |
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2 classes of drugs used for treatment of Essential Tremor
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1. Beta Blockers (Propranolol, Atenolol, sotalol, nadalol)
2. Primidone (anticonvulsant) |
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Clinical Pearl of Beta Blockers for Essential Tremor
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1. most commonly used meds
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Clinical Pearls for Primidone
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Effective for limb tremor
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